Metopirone, a blocker of the 11β-hydroxylase, was used to suppress cortisol synthesis in the eel, producing a pharmacological adrenalectomy. After 1 and 2 days, corticotropin-releasing factor (CRF) immunoreactivity was reduced in the preoptic nucleus (PON) and was increased in the rostral neurohypophysis (NH) where CRF fibers ended in close proximity to ACTH cells. After 4 days, immunoreactive (ir) CRF increased in the PON or was similar to that of controls, and was reduced in the rostral NH. It was not affected in the caudal NH among intermediate lobe (IL) ramifications. Arginine vasotocin (AVT) immunostaining was often slightly increased in the PON, but changes were not apparent in the pituitary and AVT-ir fibers remained very scarce in the rostral NH. Metopirone significantly increased the cross-sectional area of CRF-and AVT-ir perikarya in the parvocellular region and the number of these perikarya as well as the ratio of CRF to AVT cell bodies in the totality of the PON. Colocalization of CRF and AVT, barely detected in control eels, occurred in 9.6% of CRF perikarya after 1-2 days, but in only 2.4% after 4 days. ACTH cells were rapidly and markedly stimulated. These immunocytochemical studies suggest that CRF synthesis, axonal transport, and release are increased in metopirone-treated eels, acting on the pituitary to stimulate ACTH release and interrenal cell activity. The participation of AVT in ACTH cell stimulation is less clear. These data are compared to those reported in mammals. © 1990.
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